An additional P{lacW} is inserted at nucleotide 7197, in the second coding exon. This maps to the first RNA binding domain.
Neuromuscular junctions in Rbp9P2690 mutant third instar larvae have a slightly increased number of synaptic boutons in comparison with controls.
Rbp9P2690/Df(2L)ED206 adult flies do not exhibit any fusion of the mushroom body beta lobes.
Rbp9P2690/Df(2L)ED206 mutant flies do not exhibit any defects in photoreceptors or central brain neuron maintenance.
Rbp9P2690/Df(2L)ED206 mutant flies are short lived compared with controls.
Mutant flies initially perform as well as wild-type flies in a climbing assay. However, over time, the mutant flies decline in performance more rapidly than the wild-type flies, such that at 13 days after eclosion, 50% pf the mutant flies have lost their climbing ability.
Mutants show a reduction in longevity compared to wild-type controls.
Mutant adults show an increase in the penetration of fluorescently labelled beads into the brain after injection into the abdomen, indicating a defect in the blood-brain barrier.
Mutant females show 0% fertility. Phenotype is very close to the null phenotype. Ovarioles of mutant females are filled with egg chambers with abnormal numbers of cystocytes that never develop beyond a stage 6 egg chamber. Germaria are enlarged. In a few cases the ovarioles are devoid of egg chambers. As the flies age, the underdeveloped egg chambers become filled with numerous small cells (the "tumerous bag" phenotype).
Rbp9P2690/Df(2L)ED206 has short lived phenotype, non-enhanceable by Df(1)ED7165/Df(1)fneΔ
Rbp9P2690/Df(2L)ED206 is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of elav5/elavts1
Rbp9P2690 is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of elav5
Rbp9P2690/Df(1)fneΔ is a non-enhancer of abnormal neuroanatomy | embryonic stage phenotype of elav5
fneKOZ2/Df(1)fneΔ, Rbp9P2690/Df(2L)ED206 has short lived phenotype
Rbp9P2690, SxlfP7B0 has partially lethal - majority die | maternal effect | female limited phenotype
Rbp9P2690, elav5/elavts1 has lethal - all die before end of pupal stage phenotype
Rbp9P2690 has embryonic/larval neuromuscular junction phenotype, suppressible by Df(1)ED7165/Df(1)fneΔ
Rbp9P2690 has NMJ bouton phenotype, suppressible by Df(1)ED7165/Df(1)fneΔ
Rbp9P2690/Df(2L)ED206 is a non-enhancer of embryonic/larval neuromuscular junction phenotype of elav5/elavts1
Rbp9P2690 is a non-enhancer of female germline cell phenotype of Rbfox1f02600/Rbfox1e03440
Rbp9P2690 is a non-suppressor of female germline cell phenotype of Rbfox1f02600/Rbfox1e03440
fneKOZ2/Df(1)fneΔ, Rbp9P2690/Df(2L)ED206 has adult brain phenotype
fneKOZ2/Df(1)fneΔ, Rbp9P2690/Df(2L)ED206 has ribonucleoprotein granule | adult stage phenotype
Rbp9P2690/Df(2L)ED206 does not enhance the neuromuscular junction phenotypes seen in elav5/elavts1 mutant third instar larvae.
The number of boutons in the neuromuscular junctions of Df(1)fneΔ/Df(1)ED7165; Rbp9P2690/Df(2L)ED206 double mutant third instar larvae is dramatically reduced. No defects in photoreceptor or central brain neuron maintenance are observed, except for occasional vacuolizations.
Rbp9P2690/Df(2L)ED206 does not enhance the mushroom body beta lobe fusion seen in Df(1)fneΔ/Df(1)ED7165 mutant adult flies.
The axon wiring defects seen in elav5 mutant embryos is not enhanced by Df(1)fneΔ or Rbp9P2690, or both.
Removing one copy of Rbp9P2690 during oogenesis in combination with zygotic heterozygosity for SxlfP7B0 results in female lethality. No female lethality is seen in the reverse cross. This female lethality is suppressed when msl-31 is also zygotically removed.
Rbp9P2690 is rescued by Rbp9+t17.1
Rbp9P2690 is rescued by Rbp9+t17.1
The age-dependent defect in climbing ability that is seen in Rbp9P2690 flies is rescued by Rbp9+t17.1.